Evidence map›Paper›PMID 22213289›Full record

ArticleAnticancer research2012

Dual-mode interaction between quercetin and DNA-damaging drugs in cancer cells.

Temesgen Samuel, Khalda Fadlalla, Lachundra Mosley, Venkat Katkoori, Timothy Turner, Upender Manne

Open access · greenAbstract read
In one paragraph

Article in Anticancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 39 citations in OpenAlex.

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  10. Natural Polyphenols as Modulators of Etoposide Anti-Cancer Activity.International journal of molecular sciences · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Temesgen SamuelDepartment of Pathobiology, College of Veterinary Medicine, Nursing and Allied Health, Tuskegee University, Tuskegee, AL 36088, USA. tsamuel@mytu.tuskegee.edu
Khalda Fadlalla
Lachundra Mosley
Venkat Katkoori
Timothy Turner
Upender Manne
Tuskegee University · USUniversity of Alabama at Birmingham · US

Funding

TRAINING AND CAREER DEVELOPMENTU54CA118948 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI UPENDER MANNE · 2005 to 2026
$26.6M
Research Training & Career Development ProgramU54CA118638 · NCI · MOREHOUSE SCHOOL OF MEDICINE · PI Desiree Avia Rivers · 2005 to 2026
$22.7M
Research Education CoreU54CA118623 · NCI · TUSKEGEE UNIVERSITY · PI Vivian L Carter, TIMOTHY TURNER · 2005 to 2026
$20.2M
THYMIC NURSE CELL ENVIRONMENT IN PATHOGENESIS OF SYSTEMIC LUPUS ERYTHEMATOSUSG12RR003059 · NCRR · TUSKEGEE UNIVERSITY · PI ROCHON, GILBERT L. · 1988 to 2011
$13.5M
INFRASTRUCTURE IIG12MD007585 · NIMHD · TUSKEGEE UNIVERSITY · PI YATES, CLAYTON · 2012 to 2016
$4.6M
Molecular Determinants for the Bioactivity of the Flavonoid QuercetinSC2CA138178 · NCI · TUSKEGEE UNIVERSITY · PI SAMUEL, TEMESGEN · 2008 to 2010
$319k
NCI NIH HHS 2 U54 CA118948-06NCI NIH HHS SC2 CA138178NCI NIH HHS SC2CA138178NCI NIH HHS U54 CA118623NCI NIH HHS U54 CA118638NCI NIH HHS U54 CA118948NCRR NIH HHS G12 RR003059NCRR NIH HHS G12RR003059NIMHD NIH HHS G12 MD007585
6 · The paper itself

Abstract

backgroundDNA-damaging drugs constitute standard chemotherapy regimen for advanced colorectal cancer. Here, the interactions between quercetin and 5-fluorouracil (5-FU), etoposide, and camptothecin were examined in cancer cells. MATERIALS AND

methodsHCT116 colorectal or PPC1 prostate cancer cells were treated with quercetin and the drugs. Clonogenicity assays, cell cycle profiles, and expressions of p53, p21, BAX, survivin and cyclin B1 proteins were used to examine the effects of the treatments.

resultsQuercetin synergistically inhibited the clonogenicity of the wild-type cells, but inhibited the cell cycle effects of all the drugs tested. In p53-null cells, the combination of low dose 5-FU with up to 6 μM quercetin promoted clonogenic survival. Treatment of p53-wild-type cells with 50 μM quercetin reduced drug-induced up-regulation of p53, p21 and BAX. The combination of quercetin and the drugs also reduced the levels of cyclin B1 and survivin proteins.

conclusionWhile high doses of quercetin synergize with DNA-damaging agents, the effect of drug combination with quercetin is influenced by the effective doses and the p53 status of the cells.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsAntioxidantsApoptosisbcl-2-Associated X ProteinBlotting, WesternCamptothecinCell CycleCell Line, TumorCell ProliferationColorectal NeoplasmsCyclin B1Cyclin-Dependent Kinase Inhibitor p21DNA DamageDrug SynergismEtoposideFlow CytometryAntioxidantsBAX protein, humanbcl-2-Associated X ProteinBIRC5 protein, humanCamptothecinCCNB1 protein, humanCDKN1A protein, humanCyclin B1Cyclin-Dependent Kinase Inhibitor p21EtoposideFluorouracilInhibitor of Apoptosis ProteinsQuercetinSurvivinTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22213289
PMCPMC3525707
OpenAlexW2144636653

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.